Abstract. The Okinawa Trough is an incipient intracontinental back arc basin that has developed behind the Ryukyu arc-trench system. To explore its magmatic evolution and the nature of the mantle source, we present major and trace element and Sr-Nd isotopic data for mafic volcanic rocks from the Middle and Southern Okinawa Trough and the Central Ryukyu Arc. Two episodes of activity formed the latter: older (-21-13 Ma) and younger (-6-4 Ma). Although Quaternary basalts from the Middle Okinawa Trough (MOT)have major element compositions comparable to basalts from intra-oceanic back arc basins, they are characterized by relative enrichments of large ion lithophile elements and Pb and by depletions of high field strength elements analogous to those observed in Ryukyu Arc volcanics. Two components have been involved in the generation of MOT basalt, which we identify as an E-MORB type (or oceanic island basalt type) upwelling asthenospheric mantle and a"subduction component." Quaternary basalts from the Southern Okinawa Trough (SOT) have uniform Nd but heterogeneous Sr isotopic ratios and incompatible trace element compositions. This may be ascribed to more complicated tectonic and magmatic processes in the SOT compared with the MOT, such as oblique subduction of the Philippine Sea Plate and interaction with postcollisional extension in the northern Taiwan orogenic belt. Integrating geological information available from nearby regions, we emphasize that the SOT is an "atypical" back arc basin because its development essentially occurred synchronous with or even prior to development of the arc-trench system.

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Human Aurora2 was originally identi®ed by its close homology to yeast IPL1 and¯y aurora, which are key regulators of chromosome segregation and a family of serine/threonine kinases. Here we demonstrate that the Aurora2 protein is degraded rapidly after G2/M phase release in mammalian cells. Aurora2 protein has a rapid turnover rate with a half-life of approximately 2 h. In eukaryotic cells, the ubiquitin-proteasome pathway is the major mechanism for the targeted degradation of unstable proteins. The treatment of mammalian cells with proteasome inhibitors blocks Aurora2 degradation. Furthermore, Aurora2 is polyubiquitinated in vivo and in vitro using anaphase-promoting complex (APC). These results demonstrate that Aurora2 protein is turned over through the APC-ubiquitin-proteasome pathway.

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The mechanism controlling the disappearance of osteoclasts from bone surfaces after bone resorption in vivo is largely unknown. This is because there is no suitable experimental system to trace the final fate of osteoclasts. Here, we used an experimental model of tooth movement in rats to show that preexisting osteoclasts disappeared from the bone surface through apoptosis during a force-induced rapid shift from bone resorption to formation. On the distal alveolar bone surface of the maxillary molar in growing rats, many mature osteoclasts were present. When light tensional force was applied to the bone surface through an orthodontic appliance, these preexisting osteoclasts gradually disappeared. One day after the application of force, about 24% of the osteoclasts exhibited apoptotic morphology and the proportion of apoptotic cells was increased to 41% by day 2, then decreased afterward. These changes were undetectable on the control distal alveolar bone surface, which is free from tensional force. As shown by in situ hybridization, a marked increase in transforming growth factor ␤1 (TGF-␤1) and osteoprotegerin (OPG) messenger RNA (mRNA) was observed in the stretched cells on the tensioned distal bone surface, simultaneously with the loss of osteoclasts. Both of these factors are known to have a negative effect on osteoclast recruitment and survival. As early as 2 days after force application, some of these stretched cells were identified as cuboidal osteoblasts showing intense signals for both factors. Our data suggest there may be a sequential link in tensional force applied on the bone lining cells, up-regulation of TGF-␤1/OPG, and disappearance of osteoclasts. (J Bone Miner Res 2000; 15:1924 -1934)